Androgenic function was studied in seven diabetics with sexual impotence and in five patients with paraplegia. Plasma concentration of testosterone was measured before and after administration of 5,000 U. of human chorionic gonadotropin (HCG). Steroid biosynthesis by testicular tissue was studied in vitro and testicular morphology was evaluated by light and electron microscopy. The diabetic patients were also evaluated neurologically. Motor conduction velocity, electromyography of the quadriceps and the function of urinary bladder were studied. Plasma concentration of testosterone was in the normal range in basal conditions in impotent diabetics (mean 578 ± 234 mμg./100 ml.) and paraplegics (mean 788 ± 184 mμg./ 100 ml.). After stimulation with HCG, impotent diabetics showed a mean value of 1,523 ± 314 mμg./100 ml. In vitro steroid biosynthesis by testicular homogenates of diabetics and paraplegics was normal. The morphology of the interstitial tissue was normal in patients with diabetes or paraplegia. Subcellular characteristics of Leydig cells were also normal. In the tubules, a marked hypospermatogenesis with desquamation of the germinal epithelium was observed in the two groups in all patients. Alterations of the motility of the bladder were seen in six diabetics and all paraplegics. Motor conduction velocity was abnormal in the diabetics. It is concluded that in our patients androgenic function was normal, and therefare impotence can not be attributed to hormonal deficieney.

The normal weight increase of the epididymis during sexual maturation and its maintenance through adulthood were found to be dependent on the provision of androgens. Binding of [3H]dihydrotestosterone (DHT) to the epididymal 8S cytoplasmic receptor gradually decreased after castration to become undetectable after 25 days. Binding to the androgen binding protein (ABP) was absent 4 days after castration and was not reinduced by 3 weeks of testosterone (T) administration. Unilateral castration for periods of up to 27 days showed the disappearance of ABP with preservation of the 8S receptor on the castrated side, indicating a testicular source for ABP and the epididymal origin of the 8S receptor. The tissue concentrations of T and DHT in the epididymis became undetectable 30 days after castration and were restored to normal values by administration of testosterone in large doses (1.5 mg/100 g BW). Similar results were obtained in rats castrated at 10 days of age and injected with testosterone until 60 days old. The ratio DHT/T was depressed in the castrate and increased with testosterone treatment. The protein content of the epididymis (mg of protein/g wet weight) was also found to be influenced by androgens. Our results show evidence of some mechanisms involved in the trophic effect of androgens upon the epididymis and suggest the possible androgenic control of epididymal 5alpha-reductase activity. They also indicate that a testicular factor is required for the maintenance of the 8S cytoplasmic androgen receptor. It is not known whether this factor is testosterone or some other testicular secretion.

A study of steroid metabolism by a tumour of the specific gonadal stroma was carried out in a 10 year old boy. Tumours developed in the two testes from multiple foci, and clinically, no signs of sexual development were evident. Four testicular enzymes necessary for testosterone biosynthesis were estimated in the child, in two adult controls, and in three pre-pubertal boys with male pseudohermaphroditism but normal tests of Leydig cell function. 17\g=a\-Hydroxylase and 17\g=b\-hydroxysteroid dehydrogenase were similar in the five controls and in the gonad with the tumour, while 17,20-desmolase and 3\g=b\-hydroxysteroiddehydrogenase were grossly deficient in the child with the tumour. These enzyme deficiencies might explain the absence of peripheral virilization in a boy with a tumour of Leydig and Sertoli cells.